1974, British Journal of Radiology, 47, 498-500

Case reports

metaplasia are shown in areas adjacent to the diverticula. The completely metaplastic ducts have the
same histological appearance as the diverticula. The
findings therefore strongly support the view that the
diverticula derive from and represent abnormal
mucous gland ducts.
Ten cases of intramural oesophageal diverticulosis have been reported in the literature. The
patients had all experienced dysphagia for many
years. Their ages ranged from 11 to 83 years, and
there was an equal sex distribution. The following
mechanisms of pathogenesis have been suggested :
(1) The diverticula represent mucosal herniations
through the muscularis mucosa, due to increased
oesophageal intraluminal pressure (Creely and
Trail, 1970; Weller and Lutzker, 1971; Weller,
1972; Mendl, Darragh Montgomery and Stephenson, 1973). This mechanism has been linked
to the development of Rokitansky-Aschoff
sinuses in the gall-bladder (Mendl et ah,
1960).
(2) The diverticula represent hypertrophied mucosal glands, secondary to low grade infection,
possibly due to Monilia (Hodes, Atkins and
Hodes, 1966; Troupin, 1968). Review of one
case suggested that deep ulcers due to monilial
oesophagitis had initially been mistaken for
intramural diverticula (Zatskin, Green and La
Vine, 1968; Smulewicz and Dorfman, 1971).
(3) They arise from the combined effects of increased pressure and chronic inflammation (Lane,
1972).
(4) They are congenital or developmental in origin
(Culver and Chaudhari, 1967).
Based on our histological findings, we suggest
the following pathogenesis. The oesophageal gland
ducts have undergone squamous metaplasia in
response to some chronic irritation {e.g., chemical,

thermal, infective). The heaped up and desquamated

squamous cells have blocked the necks of the
glands, causing distal distension and producing the
radiologically demonstrated intramural diverticula.
The chronic inflammatory cellular infiltration may
be related to an aetiological agent, or a secondary
factor.
ACKNOWLEDGMENTS

The authors wish to thank Mr. A. J. Heriot for permission to publish this case.
REFERENCES
CREELY, J. J., and TRAIL, M. L., 1970. Intramural diverti-

culosis of the oesophagus. Southern Medical Journal, 63,

1257-1260.
CULVER, G. J., and CHAUDHARI, K. R., 1967. Intramural

oesophageal diverticulosis. American Journal of Roentgenology, 99, 210-211.

HODES, P. J., ATKINS, J. P., and HODES, B. L., 1966. Oeso-

phageal intramural diverticulosis. American Journal of

Roentgenology, 96, 411413.
LANE, J. W., 1972. Intramural oesphageal diverticulosisA
case report. Journal of the Arkansas Medical Society, 69,
87-90.
MENDL, K., DARRAGH MONTGOMERY, R., and STEPHENSON,

S. F., 1973. Segmental intramural diverticulosis associated

with and confined to a spastic area of muscular hypertrophy in a columnar lined oesophagus. Clinical Radiology, 24, 440-444.
MENDL, K., MCKAY, J. M., and TANNER, C. H., 1960.

Intramural diverticulosis of the oesophagus and Rokitansky-Aschoff sinuses in the gall-bladder. British Journal of
Radiology, 33, 496-501.
SMULEWICZ, J. J., and DORFMAN, J., 1971. Oesophageal

intramural diverticulosis: a re-evaluation. Radiology, 101,

527-529.
TROUPIN, R. H., 1968. Intramural oesophageal diverticulosis and moniliasis. American Journal of Roentgenologv,
104,613-616.
WELLER, M. H., 1972. Intramural diverticulosis of the oesophagus : report of a case in a child. Journal of Pediatrics,
80, 281-285.
WELLER, M. H., and LUTZKER, S. A., 1971. Intramural

diverticulosis of the oesophagus associated with postoperative hiatal hernia, alkaline oesophagitis and oesophageal stricture. Radiology, 98, 213-211.
ZATSKIN, H. R., GREEN, S., and LA VINE, J. J., 1968.

Oesophageal intramural diverticulosis. Radiology, 90,

1193-1194.

Lung abscess: a complication of malposition of a central venous catheter

By W. J. Norman, F.F.R.,* N. J. Moule, F.R.C.S.(Ed.), F.F.R., and E. R. Walrond, F.R.C.S.
Departments of Radiology and Surgery, University Hospital of the West Indies, Kingston 7, Jamaica
The monitoring of central venous pressure by means
of a polyethylene catheter inserted percutaneously
into the superior vena cava or right atrium is a well
established and valuable adjunct to the management
*Present address: Department of Radiology, Copthorne
Hospital, Shrewsbury SY3 8XF.

of very ill patients. These catheters are also employed

during hyperalimentation therapy for the infusion
of intravenous fluids, particularly hypertonic solutions which tend to produce thrombosis if infused
into smaller peripheral veins.
There have been several reports concerning the
complications of the use of such catheters (Langston,

498

AUGUST

1974

Case reports

1971; Smith et al, 1965; Walters, Stanger and

Rotem, 1972; Flanagan et al., 1969; Henzel and DeWeese, 1971; Swaroop, 1972).
This paper records a case of pulmonary abscess
formation due to unrecognized faulty positioning of a
central venous catheter which had passed through
the heart and entered a branch of the right pulmonary artery.
Case history

A 19-year-old man was admitted to the University Hospital of the West Indies with a small bowel fistula which
followed an operation for the relief of intestinal obstruction
at another hospital. The fistula had appeared five days
after the operation and appeared to be from the jejunum.
He was cachectic, but there was no evidence of intestinal
obstruction and it was decided to manage the patient
by restriction of oral intake and hyperalimentation intravenously. Following two weeks of satisfactory progress with
hyperalimentation through a central catheter placed via
puncture of the right cephalic vein, he suddenly developed
high fever, tachycardia, jaundice and generalized pains. A
diagnosis of septicaemia was made, and blood cultures
grew coagulase-positive staphylococci. The central venous
line was removed and replaced by another, inserted by
puncture of the left subclavian vein. Appropriate antibiotic
and hyperalimentation therapy was continued. Six days
after the insertion of the new line his condition deteriorated

FIG. 1.
Six days after the insertion of a central venous catheter
there is consolidation translucency in the right middle and
lower zones.

with the added symptoms of cough and shortness of breath,

and a chest radiograph taken at that time showed a diffuse
opacity in the right middle and lower zones which was
interpreted as representing right lower lobe pneumonia
(Fig. 1).
In spite of intensive therapy his condition continued to
deteriorate, but a further chest film taken three days later
showed almost complete clearing of the opacity. Two days
later the diffuse opacity in the right side of the chest had
reappeared and there was an area of cavitation 4 cm across
within it. A film taken following the injection of contrast
medium through the catheter is shown in Fig. 2.
The catheter is shown to have passed through the right
side of the heart and into the right pulmonary artery. The tip
is lodged in one of the branches of the middle lobe, and
there is evidence that the tip has eroded the vessel wall in
that contrast medium is seen entering the abscess cavity and
pooling in its base. Some peripheral branches of the pulmonary artery are also opacified.
The catheter was withdrawn into the right atrium following which there was a dramatic improvement in the patient's
symptoms. He subsequently underwent operation for closure of his fistula and was discharged symptom free. Resolution of the lung abscess was followed with serial chest
radiographs.
COMMENT

Apart from incorrect pressure measurements,

the chief dangers of malpositioning of a central

FIG. 2.
The abscess cavity in the right lower zone showing contrast
medium pooling in the base of the abscess. Some pulmonary
artery branches are also opacified.

499

1974, British Journal of Radiology, 47, 500-503

Case reports

venous catheter are local damage to the vessel and

perforation of its wall, or of the myocardium, and the
ectopic infusion of potentially toxic solutions.
The unreliability of clinical assessment of correct
placement of venous catheters introduced via arm
veins has recently been emphasized by Johnston
and Clark (1972) and Langston (1971). Of catheters
thought to be correctly positioned on clinical
criteria, these authors found that only 64 and 62 per
cent respectively were correctly positioned radiologically.
In this case it is apparent that the catheter was
advanced too far into the subclavian vein at the
time of its insertion, so that it passed through the
right side of the heart into a branch of the right pulmonary artery, where the tip probably wedged. Local
ischaemia was followed by inflammatory changes,
the patient being septicaemic at this time. It also
seems likely that pulmonary oedema was induced by
the direct infusion of hypertonic solutions into the
right pulmonary artery.
A prominent feature of this case was the marked
disparity between the patient's respiratory distress
and the clinical and radiological picture. His
symptoms were probably due to the direct action of
the relatively undiluted hypertonic solutions on the
lung. These signs of distress ameliorated when the
catheter was repositioned.
The appearance of fleeting opacities in the same
area of the chest in a patient undergoing hyperalimentation via a central venous catheter may suggest

the possibility of a misplaced catheter, and its

position should be checked by an injection of contrast medium.
To minimize the risk of complications the value of
serial chest radiographs has been stressed by Sullivan and Pomerantz (1969), and Land, Garrett and
Hedberg (1970) recommend the use of fluoroscopy
during the insertion of subclavian venous catheters.
REFERENCES
FLANAGAN, J. P., GRADISAR, I. A., GROSS, R. J., and KELLY,

T. R., 1969. Air embolusa lethal complication of subclavian venepuncture. New England Journal of Medicine,
281, 488-489.
HENZEL, J. H., and DEWEESE, M. S., 1971. Morbid and

mortal complications associated with prolonged central

venous cannulation. American Journal of Surgery, 121,
600-605.
JOHNSTON, A. O. B., and CLARK, R. G., 1972. Malposition-

ing of central venous catheters. Lancet, 2, 1395-1397.

LAND, R. E., GARRETT, J. C , and HEDBERG, S. E., 1970.

Television fluoroscopy and opacification of the subclavian

vein. Archives of Surgery, 101, 429-430.
LANGSTON, C. S., 1971. The aberrant central venous
catheter and its complications. Radiology, 100, 55-59.
SMITH, B. E., MODELL, J. H., GAUB, M. L., and MOYA, F.,

1965. Complications of subclavian vein catheterisation.

Archives of Surgery, 90, 228-229.
SULLIVAN, R., and POMERANTZ, M., 1969. Central venous

pressure monitoring: the subclavian approach. Surgical

Clinics of North America, 49, 1489-1490.
SWAROOP, S., 1972. Knotting of two central venous
monitoring catheters. American Journal of Medicine,
53, 386-388.
WALTERS, M. B., STANGER, H. A. D., and ROTEM, C. E.,

1972. Complications with percutaneous central venous

catheters. Journal of the American Medical Association,
220, 1455-1457.

Hyperostosis corticalis generalisatafamiliaris

By W. C. Scott, M.B., B.S., F.F.R., D.M.R.D. and T. H. T. Gautby, B.A., M.R.C.S., L.R.C.P., D.M.R.E.
Department of Radiology, Poole General Hospital, Poole, Dorset
In 1954 a curious and apparently distinct skeletal
disorder affecting a pair of adult twins was described
by Van Buchem, Hadders and Ubbens. To this
they gave the name hyperostosis corticalis generalisata familiaris. A further paper by Van Buchem,
Hadders and Hansen in 1962 gave details of seven
cases and Fosmoe, Holm and Roscoe described
an additional case, to which they gave the name Van
Buchem's Disease, in 1968. This paper presents a
further patient displaying many features apparently
characteristic of this condition.

Case history
A boy of 17 was admitted to this hospital via the accident
department having sustained an injury to his right knee in a
motor cycle accident. An X ray of this knee revealed a haemarthrosis but no bony injury. It was however observed
that the appearance of the femur, tibia andfibula,and
particularly of the epiphyses was abnormal. A number of
other areas were therefore X rayed.
The most striking radiological changes are in the skull.
There is extreme cortical thickening of the vault, particularly in the frontal and basi-occipital regions. The base
of the skull is also thickened especially in the petrous area.
The maxilla is clearly affected. Unfortunately the mandible,
which is typically involved in this condition, was not
included.

500